The recently discovered human Bocavirus has been preliminary classified into the genus Bocavirus of the family Parvoviridae. Animal bocaviruses have been known in veterinary medicine since the early 1960s. This paper reviews the current knowledge about the two eponymous members of the genus: bovine parvovirus (BPV) and canine minute virus (CnMV). In contrast to other parvoviruses, bocaviruses contain a third open reading frame in the mid of the genome encoding for a highly phosphorylated non-structural protein, NP1, whose function has not yet been determined. The VP1-unique region of BPV and CnMV contains a phospholipase A2 sequence motif. Both viruses cause diseases of the gastrointestinal and respiratory tract and are known to infect fetuses and to cause reproductive disorders. Especially young animals suffer from disease, whereas in adults subclinical infection is common. Clinical signs include diarrhea, vomiting, dyspnea, embryonic/fetal death after transplacental infection early and abortion late in gestation. Both viruses have in common that they are widespread in their host species as worldwide serosurveys indicate. For BPV it has been shown that sialated glycoproteins mediate hemagglutination reaction and function as receptor for virus attachment on permissive cells.
The demonstration of field isolates of porcine parvovirus (PPV) that differ genetically and antigenically from vaccine strains of PPV raises the question of whether the broadly used inactivated vaccines can still protect sows against the novel viruses. Ten specific-pathogen-free primiparous sows were assigned to three groups and were vaccinated with one of two vaccines based on the old vaccine strains, or served as non-vaccinated controls. After insemination, all sows were challenged with the prototype genotype 2 virus, PPV-27a, on gestation day 41; fetuses were delivered on gestation day 90 and examined for virus infection. The fetuses of the vaccinated sows were protected against disease, but both the vaccinated and the non-vaccinated sows showed a marked increase in antibody titres after challenge infection, indicating replication of the challenge virus. All sows (vaccinated and non-vaccinated) shed the challenge virus for at least 10 days after infection, with no difference in the pattern or duration of virus shedding.
Zusammenfassung:
Gegenstand und Ziel: In einer Querschnittsstudie wurde die Verbreitung von Infektionen mit dem kaninen Herpesvirus (CHV-1) und dem Canine Minute Virus CnMV) in Deutschland anhand des Nachweises von Antikörpern im Blutserum von Zuchthunden und der virologischen Untersuchung von klinischen Proben und Organmaterial verstorbener Welpen untersucht. Material und Methoden: Zwischen März 2004 und Oktober 2005 wurden 429 Serumproben im Serumneutralisationstest auf Antikörper gegen CHV-1 und im indirekten Immunfluoreszenztest (IFT) auf IgG-Antikörper gegen CnMV untersucht. Die klinischen Untersuchungsproben bestanden aus 37 Vaginalund Rachentupfern, 34 Spermaproben, 16 Kotproben sowie aus Organproben von 37 abortierten oder verstorbenen Welpen aus 14 Würfen. Alle klinischen Proben wurden mittels PCR auf CHV-1 und CnMV untersucht. Ergebnisse: 27,7% (119/429) der Serumproben wiesen neutralisierende Antikörper gegen CHV-1 auf. Die statistische Auswertung ergab nur für das Geschlecht einen signifikanten Einfluss auf den Serostatus von CHV-1. Der Anteil der Seren, die im IFT positiv auf Antikörper gegen CnMV getestet wurden, lag bei 5,7%. Die virologische Untersuchung auf CHV-1 und CnMV erbrachte in allen Fällen ein negatives Ergebnis. Schlussfolgerung: Insgesamt scheint CnMV in Deutschland deutlich weniger verbreitet zu sein als in anderen Ländern der Welt. Klinische Relevanz: Die Seroprävalenz ist nicht gleichzusetzen mit der Häufigkeit CHV-1-bedingter klinischer Erkrankungen. CHV-1 und CnMV sind wahrscheinlich in weit weniger Fällen die Ursache von Welpensterblichkeit und Reproduktionsstörungen als in der Praxis der Verdacht geäußert wird.
Since highly pathogenic avian influenza virus H5N1 emerged in 1997, avian influenza is considered one of the most important infectious diseases globally. In respect of virus transmission to humans, the consumption of raw poultry products remains of serious concern. In this study, data about survival time and inactivation kinetics of two low pathogenic avian influenza virus (AIV) strains (H3N8, H5N6) in short fermented raw sausage were obtained. In addition, the impact of the preserving factors D,L-lactic acid and sodium chloride on virus infectivity was evaluated through in vitro studies. Virus infectivity was confirmed in embryonated chicken eggs. Inactivation of H3N8 was seen in D,L-lactic acid solutions (0.15 and 0.20%, pH 4.40-4.70 and pH 3.80-3.91) at both temperatures (20 vs. 4°C) during 3 days of exposure. However, infectious virus particles could still be detected after exposure to 0.1% D,L-lactic acid (pH 5.80-5.99). In all NaCl solutions (2, 6 and 12% w/v), infectivity of the H3N8 strain decreased steadily but reduction of the virus titre increased significantly with higher temperature. In raw sausages, decline in virus titre was observed for both strains during ripening and storage. Thereby, decline of virus infectivity was dependent on time and temperature with a more marked effect at higher temperatures (22 vs. 7°C). At refrigeration (7°C), both viruses maintained infectivity over 14 days. Results indicate that appropriate processing of short fermented raw poultry sausage is likely to reduce risk of virus exposure due to adequate inactivation of AIV during ripening and storage.
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